Your browser doesn't support javascript.
loading
Chemerin attracts neutrophil reverse migration by interacting with C-C motif chemokine receptor-like 2.
Ji, Jingjing; Zhong, Hanhui; Wang, Yawen; Liu, Jinghua; Tang, Jing; Liu, Zhifeng.
Afiliación
  • Ji J; Department of Critical Care Medicine, General Hospital of Southern Theater Command of PLA, Guangzhou, 510010, China.
  • Zhong H; Department of Anesthesia, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong, China.
  • Wang Y; Department of Anesthesia, The Third Clinical College of Guangzhou University of Chinese Medicine, Guangzhou, China.
  • Liu J; Guangdong Provincial Key Laboratory of Proteomics; School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510515, China.
  • Tang J; Department of Anesthesia, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong, China. tanglitangjing@126.com.
  • Liu Z; Department of Critical Care Medicine, General Hospital of Southern Theater Command of PLA, Guangzhou, 510010, China. Zhifengliu7797@163.com.
Cell Death Dis ; 15(6): 425, 2024 Jun 18.
Article en En | MEDLINE | ID: mdl-38890311
ABSTRACT
Neutrophil reverse migration (rM) is a recently identified phenomenon in which neutrophils migrate away from the inflammatory site back into the vasculature following initial infiltration, which involved in the resolution of loci inflammatory response or dissemination of inflammation. Present study was aimed to explore the mechanisms in neutrophil rM. By scRNA-seq on the white blood cells in acute lung injury model, we found rM-ed neutrophils exhibited increased gene expression of C-C motif chemokine receptor-like 2 (Ccrl2), an atypical chemokine receptor. Furthermore, an air pouch model was established to directly track rM-ed neutrophils in vivo. Air pouches were generated by 3 ml filtered sterile air injected subcutaneously for 3 days, and then LPS (2 mg/kg) was injected into the pouches to mimic the inflammatory state. For the rM-ed neutrophil tracking system, cell tracker CMFDA were injected into the air pouch to stain the inflammatory loci cells, and after 6 h, stained cells in blood were regarded as the rM-ed neutrophil. Based on this tracking system, we confirmed that rM-ed neutrophils showed increased CCRL2. We also found that the concentrations of the CCRL2 ligand chemerin in plasma was increased in the late stage. Neutralizing chemerin decreased the rM-ed neutrophil ratio in the blood. These results suggest that circulating chemerin attracts neutrophils to leave inflammatory sites by interacting with CCRL2, which might involve in the dissemination of inflammation.
Asunto(s)

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Movimiento Celular / Quimiocinas / Péptidos y Proteínas de Señalización Intercelular / Neutrófilos Límite: Animals / Humans / Male Idioma: En Revista: Cell Death Dis Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Reino Unido

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Movimiento Celular / Quimiocinas / Péptidos y Proteínas de Señalización Intercelular / Neutrófilos Límite: Animals / Humans / Male Idioma: En Revista: Cell Death Dis Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Reino Unido